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UVEITIC GLAUCOMA

UVEITIC GLAUCOMA. TARIQ ALASBALI, MD. PDS PXF HEMOLYTIC PHACOLYTIC INFLAMMATORY ↑ EVP. PUPILLARY BLOCK PLATEAU IRIS. POAG JUVENILE. PUSHING. PHACOMOROHIC ECTOPIA LENTIS APHAKIC PSEUDOPHAKIC INFLAMMATORY PS AQ MISSDIRECTION SUBRETINAL MASS. AXIAL SHALLOWING

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UVEITIC GLAUCOMA

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  1. UVEITIC GLAUCOMA TARIQ ALASBALI, MD.

  2. PDS PXF HEMOLYTIC PHACOLYTIC INFLAMMATORY ↑ EVP PUPILLARY BLOCK PLATEAU IRIS POAG JUVENILE PUSHING PHACOMOROHIC ECTOPIA LENTIS APHAKIC PSEUDOPHAKIC INFLAMMATORY PS AQ MISSDIRECTION SUBRETINAL MASS • AXIAL SHALLOWING • CHOROIDAL EFFUSION • CHOROIDAL HE • AQ MISSDIRECTION • ROP • PHPV • CHOROIDAL MASS PERIPH SHALLOWING IRIS CYST CB CYST CB SWELLING SULFA PRP CB INFLAMMATION CB TUMOUR PULLING PAS FORMATION NVG INFLAMMATION TRAUMA TUMOUR RELATED MEMBRANEGROWTH ICE EPITH DOWNGROWTH FIBROUS INGROWTH

  3. Uveitis Classifications • Anatomic Classification • Duration Classification

  4. Uveitis Classifications I) Anatomical Classification: • Anterior • Intermediate (Pars planitis 85%, MS, sarcoid, TB, lyme, toxoplasmosis, toxocariasis, syphilis, IBD (children) lymphoma, Eale’s) • Posterior • Panuveitis (ant + intermediate + post)

  5. Anatomical Classification:

  6. Q1: Which form of ocular inflammation (anatomical classification) most frequently produces an IOP elevation?

  7. A1: Anterior uveitis (chronic >>> acute) Even glaucomas that result from other types of ocular inflammation are usually the consequence of secondary involvement of the anterior uveal tract.

  8. Q2. What are typical IOPs in anterior uveitis?

  9. Q2. What are typical IOPs in anterior uveitis? A2. LOW secondary to CB shut down +/- increased uveoscleral outflow

  10. Uveitis ClassificationsII) Duration Classification: Acute: Usually anterior uveitis Sudden onset Moderate ocular pain Photophobia Blurred vision IOP often LOWER than other eye • Sub-acute: • Often minimal symptoms • often undetected till significant complications • Chronic: longer than 3 months • Most likely to have ↑ IOP

  11. Acute Anterior Uveitis • 0.2% cumulative lifetime incidence in general population • HLA-B27 positive • 50% of cases in white patients (Lancet 1973; 2: 944) • Younger age onset (median early 30s) (AJO 1995; 120:351) • Male > female (AJO 1995; 120:351) • Unilat or unilat alternating > bilat (AJO 1995; 120:351)

  12. BEHÇET’S DISEASE • Idiopathic multisystem disease • More common in men • Occurs in 3rd - 4th decade • Associated with HLA-B5

  13. BEHÇET’S DISEASE • Incidance: • 1/100, 000 prevalence in USA • 670/100,000 in Japan • BD is most prevalent (and more virulent) in the Mediterranean region, Middle East, and Far East, with an estimated prevalence of 1 case per 10,000 persons

  14. BEHÇET’S DISEASE Aetiology • Unknown • Various bacteria and viruses suggested • No good evidence to suggest any of them • Tumour necrosis factor (TNF) thought to be important

  15. BEHÇET’S DISEASE Systemic Involvement • Oral aphthous ulceration – 100% • Genital ulceration – 90%

  16. BEHÇET’S DISEASE Systemic Involvement • Skin lesions – 80% • Erythema Nodosum • Acneiform • Uveitis 70% (inflam. of iris, ciliary body or choroid)

  17. BEHÇET’S DISEASE Systemic Involvement • CNS involvement – strokes • Major vessels SVC obstruction • Increased skin response to trauma

  18. BEHÇET’S DISEASE Ocular Features • Acute iritis • Pain, redness & VA • Flare • Inflammatory cells in anterior chamber • KPs • Recurrent hypopyon (Fluid level of WBC)

  19. BEHÇET’S DISEASE Ocular Features • Marked inflammation of the eye • Retinal vasculitis and haemorrhage • Occlusive periphlebitis (venous sheathing & occlusion) • Cataract or glaucoma

  20. BEHÇET’S DISEASE diagnosis International criteria published in 1990 require Oral ulcers 3 X /1 year + Any 2 of the following: • Recurrent genital ulcers • eye lesions • Skin lesions • Positive pathergy test 2mm plus papule developing over 24-48 hrs after oblique insertion of a 20 gauge needle into skin.

  21. Sarcoidosis • Multisystem inflammatory disorder • Unknown origin • Young adults • Black • Histopathology: noncaseatinggranulomas • Systemic involvement: • Hilarlymphadenopathy, • Peripheral lymphadenopathy, • Cutaneous lesions • 38-50% have ocular involvement (AJO 1978; 86:648 & Jpn J Ophthalmol 1992; 36:452)

  22. Sarcoidosis – Anterior Uveitis • Most common ocular manifestation = chronic granulomatous uveitis • Mutton fat KPs (15%) (AJO 1978; 86:648) • Bilateral > unilateral • Iris nodules (11.4-35%) (Ophthalmology 1986; 93: 511) • AC angle nodules (49%) (Ophthalmology 1986; 93: 511) • CB nodules (42%) (Ophthalmology 1986; 93: 511)

  23. Sarcoidosis – Anterior Uveitis • Glaucoma in 11% with ocular sarcoid(AJO 1978; 86:648) • Glaucoma in 34% with ocular sarcoid (Jpn J Ophthalmol 2002;46:556-62 ) • Most common mechanism of glaucoma : - obstruction of TM with inflammatory debris or nodules (Ann NY AcadSci 1976; 278:445) • Other mechanisms: Inflammatory cell infiltration around the inner and outer walls of Schlemm’s canal Iris bombe with PAS formation NVI and NVA

  24. Features • Described in 1948 by Posner and Schlossman • “Glaucomatocylitic crisis” characterised by self-limited recurrent episodes of markedly elevated IOP with mild AC inflammation • IOP elevation out of proportion to degree of AC inflammation • Usually in adults 20-50 yrs • Previously thought to be idiopathic, but postulated aetiologies include • Abnormal vascular process • Autonomic defect • Infective: HSV, CMV

  25. Features • Chronic unilateral (bilateral in 10%) iridocyclitis • Classic triad of • Iris heterochromia • KPs • Cataract • Low grade inflammation which does not usureq Rx • Postulated aetiology • Adrenergic dysfunction • Infective cause: link between ocular toxoplasmosis and FHI • Immunologic theories

  26. JIA • Monoarticular or pauciarticular or polyarticular. • F>M • RAF –ve ,ANA,HLA-B27. • The most common systemic disease associated with uveitis in children. • Iridocyclitis in 30% of pauciarticular. • Arthritis then uveitis. • Under treatment by ophthalmologists → PS + PAS formation → closed angle glaucoma • Glaucoma===>14 -27% of JRA.

  27. Uveitis Masqueraders (i.e. cells in the AC with ↑ IOP but not uveitis) • Infection (chronic endophthalmitis) • Tumors (lymphoma, melanoma) • Acute angle closure • Neovascular glaucoma • Secondary reaction to intraocular FB

  28. First reported by: Joseph Beer in -------- 1813 Desmans in -------- 1821 Mackenzie in -------- 1830 Glaucoma Associated with Uveitis

  29. Glaucoma Associated with Uveitis 391 eyes F/U median 55 months • Etiology of uveitis: • Topographic Types Difference non-significant [P>0.05] • Incidence • 6.6% at 1 year • 11.2% at 4 years • 22.7% at 10 years • Conclusion: • Presence of glaucoma was associated with an increasing risk of visual loss. • The incidence of glaucoma increased with time and similar among • different types of uveitis. Neri P. J Glaucoma 2004;13:461-65

  30. Secondary Glaucoma in Uveitis Patients Clinical Entry Uveitis Secondary Glaucoma Patients % Affected eyes (A) Eyes (B) B/A x 100 (%) HTLV – 1 uveitis 194 17.7 260 42 16.2 Vogt-Koyanagi-Harada’s disease 107 9.7 214 35 16.4 Ocular toxoplasmosis 85 7.7 95 11 11.6 Sarcoidosis 71 6.5 129 44 34.1 Behcet’s disease 55 5.0 96 20 20.8 Herpetic anterior uveitis 22 2.0 23 7 30.4 HLA-B27-related acute anterior uvietis 21 1.9 25 5 20.0 Posner-Scholossman syndrome 10 0.9 10 10 100* Others 92 8.4 116 23 16.1 Idiopathic uveitis 442 40.2 636 96 15.0 TOTAL 1099 100 1604 29318.3 *HTLV-I: human T-lymphotropic virus type1. HLA: human leukocyte antigen Takahashi T et al. Jpn J Ophthalmol 2002;46:556-62

  31. Glaucoma Associated with Uveitis • 25% of uvetic patients: Ocular hypentensive • 5-19% of uveitic patients: Develop S.G.

  32. Risk factors for elevated IOP in uveitis patients JIA, and ANA positive uveitis without evidence of arthritis. • Chronicity • Age • Corticosteroids • Activity seqandary glaucoma in children with uveitis Sijssens et al. Ophthalmology 2006;113:853-9 Herbert H et al. J. Glaucoma 2004;13:96-99

  33. PATHOGENESIS • Biochemical and Cellular Changes in Aqueous Composition • Direct Involvement of the TM • Corticosteroids Effects on the TM • Morphologic Changes in the AC Angle • Proteins • Inflammatory Cells • Prostaglandins • Inflammatory Mediators (Cytokines) & Toxic Agents

  34. PATHOGENESIS • Biochemical and Cellular Changes in Aqueous Composition uveitis Normal aqueous content is 1% of that in the serum permeability of blood-aqueous barrier (non-specific) 1.Proteins proteins in the aqueous (resembles undiluted serum) Persistent Affects IOP • Indirectly • Post synechiae & PAS • Directly • Aqueous sludging, impeding outflow

  35. PATHOGENESIS Biochemical and Cellular Changes in Aqueous Composition 2.Inflammatory Cells Affects IOP Indirectly By releasing inflammatory mediators, altering TM cells size, function and extra-cellular matrix composition. Directly Infiltrate TM and SC causing mechanical blockage

  36. PATHOGENESIS Biochemical and Cellular Changes in Aqueous Composition 3.Prostaglandins • Affects IOP • Prostaglandins E1 & 2 IOP • Prostaglandins F2 αIOP

  37. PATHOGENESIS Biochemical and Cellular Changes in Aqueous Composition 4.Inflammatory Mediators (Cytokines) & Toxic Agents Interleukin-1 Conventional root IOP

  38. PATHOGENESIS • Direct Inflammation of the TM • Posner-sehlossman Syndrome • Fuchs’ Uveitis • Herpetic Keratouveitis

  39. PATHOGENESIS • Effect of Corticosteroids on the TM • 35% of normal population, moderate responders • 4-6% high responders (>15mmHg) • 50% or more of POAG population, high responders Increase the aqueous production Affects IOP Reduction of aqueous outflow BY • Alteration in cell size • Cytoskeletal organization • Extra-cellular matrix deposition • Weireb RN et al. Invest Ophthalmol Vis Sci 1985;26:170-5 • Levin DS, et al. Am J Ophtalmol 2002;133:196-202 Veda J et al. Invest Ophthalmol Vis Sci 2003;44:4772-9 Velota et al. Curr Opn Ophthalmol 2004;15:136-140

  40. Incidence of steroid responsiveness

  41. PATHOGENESIS • Morphologic Changes in the Anterior Chamber Angle • Open Angle Uveitic Glaucoma • Mechanical blockage to outflow pathways • Chronic inflammatory damage to outflow pathways • Trabeculitis • Steroid-induced

  42. PATHOGENESIS • Morphologic Changes in the Anterior Chamber Angle • Angle Closure Uveitic Glaucoma

  43. Uveitic Glaucoma Management • Evaluation • History & Symptoms • Visual function (perimetry) • Slit-lamp: Etiology clues • Gonioscopy: Classification • Fundus biomicroscopy: Clues, C/D, NFL • UBM: Iridocorneal angle, Ciliary body Proper Diagnosis Proper Diagnosis

  44. Uveitis Work Up • CBC + differential • HLA • ESR + CRP • ACE, lysozyme • CXR +/- CT chest • FTA Abs + VDRL • TB skin test • Titers: toxocariasis, toxoplasmosis, lyme

  45. Management • Control Inflammation: Undertreating uveitis with corticosteroids to minimize IOP elevation at the expense of good control of inflammation is A false economy

  46. Management • Medical therapy: • Beta-blockers • CA inhibitors • Adrenergic agonists • Prostaglandin analogues? • Miotics - Avoid

  47. Q3: What glaucoma drops have been associated with uveitis?

  48. A3: Brimonidine (AJO 2000; 130:287) Metipranolol (AJO 1997; 123:843) prostaglandin analogues (Surv Ophthalmol 2002; 47 (suppl 1): S219)

  49. Management • Surgical: • Laser therapy - Laser iridotomy (pupillary block) - ALT – ineffective (avoid it) • Filtering surgery - Trabeculectomy with antimetabolite - Non-penetrating glaucoma surgery - Tube surgery - Goniotomy • Cyclodestructive procedures

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